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Scientific Approach to the Treatment of Acne Vulgaris

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Scientific Approach to the Treatment of Acne Vulgaris Scientific approach to the treatment of acne vulgaris Acne vulgaris is a dermatosis which involves the pilosebaceous apparatus of the skin; namely, the sebaceous gland and hair follicle (Fig. 1). Wilma F. Bergfeld, M.D Clinically, the skin changes are those of increased Department of Dermatology numbers of comedones (blackheads), milia (white- Department of Pathology heads or closed comedones), inflammatory papulo- pustular lesions, cysts, and atrophic or hyper- trophic scars. These acne lesions are most fre- quently observed on the face and less frequently on the chest and back. This distribution follows the embryonic development of the sebaceous gland with the greater number of glands being distributed over the face and lesser number and smaller glands distributed over the scalp, chest, and trunk. Acneform lesions may involve other areas such as arms, legs, and intertriginous skin. Acne vulgaris has been associated with other dis- eases of the pilosebaceous apparatus such as seborrheic dermatitis of the face and scalp, dis- secting folliculitis of the scalp, and hidradenitis suppurativa predominately of the axilla and groin.1 Recognition and treatment of these asso- ciated entities result in concomitantly good re- sponse to therapy. The onset of acne vulgaris is usually associated with the increased androgen stimulation of the sebaceous follicle which occurs either prepuber- tally or at puberty. Acneform lesions develop in 277 Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. 278 Cleveland Clinic Quarterly Vol. 42, No. 1 SEBACEOUS FOLLICLE SEBACEOUS GLAND HAIR DERMIS PILOSEBACEOUS APPARATUS Fig. 1. Drawing shows pilosebaceous apparatus of the skin. 42% of girls and 36% of boys between lesions develop.3 The inflammatory the ages of 8 and 10 years,2 and in the lesions, papulopustular and cystic, remainder of the adolescent group produce moderate to severe destruc- acneform lesions develop between the tion of the dermis of the skin which ages of 10 and 15 years. Acne vulgaris, eventuates in scarring of the involved a disease of the adolescent, is relatively area (Table 1). Both the inflammatory self-limited, but on occasion it will lesion and the scar are unacceptable to continue into adulthood. the young adolescent. Good results can Clinically, acne vulgaris can be be obtained by removing the primary divided into two major types: inflam- lesions by mechanical extraction and matory and noninflammatory. The acne surgery, which prevent the for- noninflammatory lesions, the come- mation of the more severe inflamma- done and milium, are primary lesions tory acne lesions. of acne from which the inflammatory Pathogenesis of acne Table 1. Classification of acne The pathogenesis of an acne lesion is influenced by many factors. How- Type of acne Severity ever, the major, local etiologic factors involve the pilosebaceous apparatus. Noninflammatory Minor These are (1) abnormal keratinization Comedones 4 6 Milia of the sebaceous follicle, " (2) the 7 11 Inflammatory Intermediate presence of microflora, " which pro- Papulopustular Moderate duce a lipase capable of breaking down Cystic Moderate-severe the normally secreted sebum into a Cystic-erosive n 12 short-chain fatty acid, C10 to C18 ' Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. Winter 1975 Treatment of acne vulgaris 279 Abnormal Follicular Keratinization Microflora Sebum Fig. 2. Diagram shows factors that influence the pathogenesis of acne. (Fig. 2). This fatty acid is extremely triglycerides, and less important irritating to the surface of the skin and squalene. has been known to cause an irritant The inflammatory lesions observed reaction when released into the dermis, under light microscopy develop from resulting in an inflammatory acne the leakage of horny materials, fatty lesion (Table 1). acids, and microflora into the support- The keratinizing epithelium of the ing connective tissue and dermis, with sebaceous follicle demonstrates in- a resulting intense inflammatory reac- creased rate of keratinization of cohe- tion composed of polymorphic leuko- sion of the horn cells. This cohesive- cytes, macrophages, giant cells, tissue ness reduces normal shedding and necrosis, and later fibrosis. The forms an impaction (open or closed) greatest amount of fibrosis and necrosis comedone. The impaction can be ex- is in the acne vulgaris major type and aggerated by stomal edema which is results in atrophic or hypertrophic frequently seen in the premenstrual scars on healing. female. The microflora cultured from the Therapeutic approaches keratogenous debri (horn) are Coryne- The therapy of acne vulgaris is bacterium acnes, the most prominent directed toward the known etiologic and important organism, staphylococci factors and occasionally to the lesser (12 varieties), and Pityrosporum ovale contributing factors. The major fac- and orbicularis. The latter two aerobes tors are again abnormal keratiniza- are found in superficial portions of the tion and microflora with lipase activi- infundibulum of the follicle; the an- ties which produce an irritating aerobic diphtheroid, C. acnes, is found short-chain sebum lipid (Table 2). colonized between the lamellar con- The primary acne lesions, come- centric rings of the horny material done and milium, result from abnor- within the comedone. All of these mal keratinization of sebaceous follicle organisms demonstrate a lipase activity and can easily be removed by mechani- which is capable of splitting the lipid cal extraction. This technique can be sebum into short-chain fatty acids, taught to patients so that it can be Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. 280 Cleveland Clinic Quarterly Vol. 42, No. 4 Table 2. Treatment of acne vulgaris agents; and salicylic acid prepara- tions.15 Precipitated sulfur solutions Acne minor Topical agents should be avoided since they are 16 Lipid surfactants mildly comedogenic. Vitamin A acid 0.05% to 0.1% cream, The reduction of the normal micro- 0.25% gel flora and the lipase activity of these Acne surgery organisms is extremely helpful in con- Ultraviolet light Drying-oxidizing agents : benzoyl perox- trolling inflammatory acne, intermedi- ide ate and major types. This can be done Antiseborrheic shampoo by topical and systemic therapy. Topi- Acne intermediate cal therapy includes antibiotic solu- Minor + tion, 2% erythromycin alcohol solu- Topical antibiotic solution Parenteral maintenance antibiotics tion, which has been clinically effective 17 (TCN) in reducing the inflammatory lesion; Cryotherapy benzoyl peroxide, an oxidizing agent, Acne major has also been a successful topical Minor + intermediate + agent. The action of the latter ap- Corticosteroids, parenteral Cryotherapy—selected cases pears to dry and oxidize the inflamma- Avoidance of ultraviolet light tory lesion and destroys the anaerobic lipase producer or C. acnes. Since the done at home. By eliminating the pri- C. acnes is the most significant lipase mary lesion one prevents the forma- producer in the inflammatory lesion, tion of an inflammatory acne lesion, control of the number and the lipase papulopustular or cystic.13 Another activity of this diphtheroid definitely topical agent that removes the primary improves the acneform eruption. lesion is vitamin A acid (0.05% to Tetracyclines, erythromycin, and 0.1%) in an alcohol wipe or cream. minocycline administered parenterally This agent, when applied to the skin are also effective agents in treating the daily, reduces the abnormal keratiniza- inflammatory acne of intermediate to tion occurring in the sebaceous follicle, major types.18-20 These antibiotics and thus prevents the formation of reduce the lipase activity and coloni- comedones and milia.14 It is not zation of the microflora even when particularly effective against the in- administered in 50- to 250-mg mainte- flammatory lesions. Vitamin A has nance doses daily.19 Tetracyclines ad- long been used parenterally in doses of ministered to adolescents younger 50,000 to 100,000 I.U. daily for treat- than age 11 is contraindicated because ment of acne vulgaris minor type. This of permanent discoloration of the sec- has been clinically helpful, but double- ondary teeth. blind studies have not supported the Since the evolution of the acneform clinical impression.2 lesion is indirectly related to the size Irritating acnegenic surface lipids and function of the sebaceous gland of the skin may be removed by topical and its production of sebum, it is pos- use of lipid solvents; cleansing agents, sible to control acne vulgaris by con- in the form of soaps, detergents, astrin- trolling the sebaceous gland and its gents, nonionic solutions, abrasive sebum production. This has been Downloaded from www.ccjm.org on September 27, 2021. For personal use only. All other uses require permission. Winter 1975 Treatment of acne vulgaris 281 done effectively by the use of estrogen Table 3. Precipitating factors, agents products parenterally, which appear to inhibit the androgen stimulation of Hormones (androgen) the sebaceous gland.21-23 The most Hereditary Topical irritants, soaps, precipitated sulfur commonly used estrogen products are coal tar, chlorinated hydrocarbons easily obtained as birth control pills, Systemic drugs, halogens, high dose steroids diethylstilbestrol and Premarin. In Physical agents, cobalt therapy selecting a particular estrogen product, Tissue
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